Abstract

Intracerebroventricular morphine consistently inhibited spontaneous urinary bladder contractions recorded from the anesthetized rat. This effect was reversed by naloxone and appeared to be exerted within the forebrain. Neither dynorphin-(1-13) nor U-50, 488 (kappa-agonists) affected bladder motility. Ethylketocyclazocine inhibited contractions only at higher doses, possibly due to mu-receptor interactions. Bladder activity was consistently inhibited by the mu-agonists morphiceptin and [D-Ala2, MePhe4, Gly-(ol)5]enkephalin (DAGO) and by [D-Ala2, D-Leu5]enkephalin (DADLE, delta-agonist). DAGO was the most potent compound tested. These observations support the involvement of mu- and possibly delta-receptors in the centrally mediated inhibition of urinary bladder motility by opioids.